Background: Percutaneous myocardial laser (PML) reduces symptoms in patients with intractable angina. PML leads to a certain loss of viable myocardium, we therefore assessed if troponin or cardiac markers release may explain the clinical effect, and furthermore assessed the markers release during percutaneous sham procedures.
Methods: Eighty-two patients with chronic refractory angina were randomized to either percutaneous myocardial laser or a true sham procedure. Cardiac markers were assessed before the procedure, and (1/2), 2, 4, 6, and 10-12 h postprocedure.
Results: Troponin I increased to median peak levels (range) of 4 (0.6-43) microg/L in the laser group vs. 1.5 (0.1-5.9) microg/L, p=0.001, and creatine kinase MB to 14 (6-357) microg/L vs. 11 (3-40) microg/L, p<0.05, within and between-group comparison, the rise of CK-MB occurred significantly earlier in the sham group, 3.8 vs. 2.5 h. A time-dependent between-group difference was only detected for troponin. 88% of sham and 100% of laser patients had marker levels above reference limits. There was no correlation between the number of laser/sham created channels, biomarker levels postprocedure, and changes in left ventricular ejection fraction or angina improvement during 12 months of follow-up.
Conclusions: The release of cardiac markers is not related to relief of angina after myocardial laser. The use of intracardiac catheters induces a considerable marker release, which is not caused by acute ischemia.